Congestive heart failure is a major disease with a high mortality rate. The disease progresses continuously, the causes being compensation of the heart muscle to make up for the loss of function due to ischemic (i.e., restriction in blood supply) and infarcted (i.e., necrotic tissue resulting from restriction in blood supply) myocardium, mechanical deformation of weakened wall structures, valve regurgitation and other disease states. As the heart compensates, over-working the still functioning regions of the myocardium, more tissue becomes ischemic and infarcted, and the heart chamber expands in size due to weakened infarcted regions until the anatomical valve structures can no longer operate properly.
In other cases, the wall of the heart thickens to the point that the ventricle(s) are no longer able to effectively dilate to fill properly and/or to contract properly. The resulting complications due to low cardiac output and pulmonary hypertension become progressively more debilitating, leading to death. Existing methods for treating congestive heart failure include drugs to control heart rate, blood volume, myocardial contractility and/or blood pressure, the removal of infarcted or hypertrophied tissue/ventricular re-sectioning, valve repair and/or valve annular re-shaping and the mechanical constraint of the heart chamber.
Another approach for treating ischemic or infarcted myocardial tissue is the implantation of cells, such as mesenchymal stem cells, skeletal myoblasts, bone marrow mononuclear cells, etc., which will facilitate the revitalization of ischemic and/or infarcted heart tissue. Other approaches include the injection of a gene or a gene(s) in vectors/delivery micelles to cause local cells to produce substances to control the growth of desired tissues such as myocardium and/or blood vessels. Other approaches also include the injection of a stabilizing, reinforcing or bulking material(s) into infarcted and/or thinned tissue to mechanically reinforce it, such that its expansion/thinning, and the resulting expansion of the ventricular volume, may be slowed or halted. Two or more of these approaches may be combined. Hereafter, these types of materials, as well as solutions containing them, will be referred to as therapeutic agents.
The injection approach may utilize a catheter like the one described in U.S. Patent Application No. 2005/0070844, “Deflectable Catheter Assembly and Method of Making Same,” incorporated herein in its entirety. The catheter may include a distal deflecting portion, which has a needle that may be extended or retracted from its distal tip. Due to the highly dynamic nature (e.g., wall motion) of the beating heart and the difficulties in externally visualizing a catheter placed therein, the stability of the catheter tip with respect to the heart wall may be difficult to determine.
One existing approach used to indicate a successful needle penetration into ventricular tissue is to detect a premature ventricular contraction (PVC) after extending the needle. In other words, this approach assumes that a PVC will be triggered by the needle penetrating the heart wall. This approach is problematic for several reasons. One is that a PVC may occur for a number of reasons besides needle penetration (e.g., stress, caffeine and dehydration may increase the heart's sensitivity/likelihood of producing spontaneous PVC's and typically, excessive mechanical deformation of the heart muscle, such as by a needle or a catheter tip, may produce a PVC), which results in false positives. In other words, a PVC may occur when a needle penetration is attempted, when in fact the needle penetration was unsuccessful and the PVC was triggered by the deformation of the heart muscle as the needle was extended. Another problem is that healthy and ischemic tissue does not always generate a PVC upon needle penetration. Yet another problem is that dead or scar tissue does not generate a PVC. As a result, the region of treatment may receive more damage than it might otherwise (e.g., due to repeated penetrations after a false negative) or not be treated at all (e.g., due to lack of needle penetration).
Generally, a cardiac catheter is used in a catheter lab facility, or cath lab. Such labs are crowded with equipment and people involved in the catheterization procedure, such as physicians, assistants, and, of course, the patient. Information recorded by, for example, electrodes disposed at the distal end of a catheter travels through wires in the catheter out of the patient's body and then, through a wired connection, to a data processing system in order to display the electrode data to the physician, assistant, etc. This multitude of wires further crowds a crowded lab and the sterile work area/the area of the patient near the catheter insertion site which impairs the efficiency of the medical practitioners. FIG. 13 illustrates the wired system. Electrodes 1305 disposed on the distal end of catheter body 1310 transmit data through wires in catheter body 1310 back through handle 1315 outside the patient into an electrical junction 1320. From junction 1320, data travels over a wired connection to data processing system 1325 which displays the electrode data in the form of an ECG. Additionally, if the catheter must be rotated during use (a requirement of a needle injection catheter used to treat a ventricle of the heart), then the wired connections between the catheter handle 1315 and data processing system 1325 will become twisted and possibly fail or become tangled with other cath lab devices, if special care is not taken.